Professor Andy Clark PhD

• PhD, Department of Medicine, University of Birmingham (1992)
• BA (Hons) Natural Sciences (Genetics), University of Cambridge, UK (1987)

Andy Clark studied Natural Sciences at the University of Cambridge before doing a PhD in transcriptional regulation of insulin genes at the University of Birmingham. He continued his research at the University of Birmingham for two years, funded by a fellowship from Diabetes UK, before moving to the Cancer Research UK labs in Lincoln’s Inn Fields for three years.

He then worked for almost sixteen years at the Kennedy Institute of Rheumatology, Imperial College London, first as a lecturer, then senior lecturer, then reader. In 2012 Andy was appointed as Professor of Inflammation Biology at the University of Birmingham.

• Immunology and Immunotherapy MSc - Module lead for Inflammation and Cell Migration
• Biomedical Science BSc - three lectures in “Cellular Pathology” and “Rheumatology and Orthopaedics” modules

• Andy supervises laboratory-based research projects for the MSc in Immunology and Immunotherapy
• Andy has supervised thirteen PhD students to award of degree. Most of these students are still in medical or scientific careers, some in industry, others in academia

Andy is interested in supervising doctoral research students in the following areas:

• Transcriptional and post-transcriptional gene regulation in the inflammatory response
• The biology of macrophages in the rheumatoid synovium
• Anti-inflammatory mechanisms of action of glucocorticoids and interleukin 10

If you are interesting in studying any of these subject areas please contact Professor Andy Clark directly, or for any general doctoral research enquiries, please email mds-gradschool@contacts.bham.ac.uk.

For a full list of available Doctoral Research opportunities, please visit our Doctoral Research programme listings.

Research themes

Inflammation, Resolution, Rheumatology, Gene expression.

Research activity

Control of mRNA stability

Inflammatory mediators such as tumour necrosis factor a (TNFa) are potentially harmful. Their expression is tightly regulated and normally occurs in a transient manner, with rapid induction by a pro-inflammatory stimulus followed by a rapid return to baseline. This pattern of gene expression is dependent on dynamic regulation of mRNA stability. We have characterised a phosphorylation-mediated switch that controls the stability of TNFa and many other pro-inflammatory mRNAs. We recently showed that this switch can be targeted to prevent different forms of experimentally-induced inflammatory pathology. Translational implications of these discoveries are being explored.

Feedback nodes

Resolution of inflammation is partly dependent on negative feedback loops, which ensure that responses to pro-inflammatory stimuli are both transient and proportional. For example, pro-inflammatory stimuli activate the MAPK p38 signalling pathway, promoting expression of inflammatory mediators such as TNFa At the same time, the expression of Dual Specificity Phosphatase 1 (DUSP1) is induced. DUSP1 inactivates p38 to terminate the inflammatory response. Negative feedback mechanisms such as this can also be exploited by anti-inflammatory agonists. For example, the expression of DUSP1 is enhanced and extended by anti-inflammatory glucocorticoids, and this results in more rapid and effective inactivation of inflammatory mediator gene expression. We refer to genes that behave like DUSP1 as “Feedback Node Genes”. Their cooperative regulation by both pro- and anti-inflammatory stimuli is poorly understood, but seems to play a major role in limiting inflammation and preventing chronic inflammatory pathology. We are investigating various Feedback Node Genes and trying to understand the basis of their cooperative regulation.

• Member of the Population and Systems Biology Board of the Medical Research Council
• Member of the Editorial Board of the Journal of Biological Chemistry
• Member of the Science Committee of the Society for Endocrinology